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J Thorac Cardiovasc Surg 1997;114:635-642
© 1997 Mosby, Inc.

CARDIAC AND PULMONARY REPLACEMENT

DIBUTYRYL CYCLIC ADENOSINE MONOPHOSPHATE ATTENUATES LUNG INJURY CAUSED BY COLD PRESERVATION AND ISCHEMIA-REPERFUSION

Received for publication Jan. 30, 1997 revisions requested May 7, 1997; revisions received May 27, 1997 accepted for publication May 28, 1997. Address for reprints: Hiromi Wada, MD, Department of Thoracic Surgery, Chest Disease Research Institute, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606, Japan.

Abstract

Objective: Dibutyryl adenosine 3`,5`cyclic monophosphate (db-cAMP) is a membrane-permeable analog of adenosine 3`,5`cyclic monophosphate (cAMP). We examined the effect of db-cAMP against lung injury caused by cold preservation and ischemia-reperfusion. Methods: Rats were divided into three groups (each n = 6) according to the presence or absence of db-cAMP in the preservative solution and cold ischemia (4° C for 15 hours). In the fresh group, the lung was flushed with the preservative solution and reperfusion was performed immediately. In the control group and the db-cAMP group, the lung was flushed either with the solution or with a combination of the solution plus db-cAMP, respectively, and preserved at 4° C for 15 hours. The lung was reperfused for 60 minutes in an ex vivo rat lung perfusion model. Results: The shunt ratios of the reperfused lung in the db-cAMP group were 4.0% ± 1.6% and 3.4% ± 1.2% 10 and 60 minutes, respectively, after the initiation of reperfusion, being as low as those in the fresh group and significantly lower than those in the control group (p < 0.01). The wet/dry weight ratio of the lung tissue after reperfusion was 5.99 ± 1.50 in the db-cAMP group, which was similar to that in the fresh group (5.45 ± 0.23) and significantly lower than that in the control group (14.20 ± 3.43) (p < 0.01). Electron microscopic examination showed less damage in the pulmonary arterial endothelium in the db-cAMP group. Conclusions: We conclude that db-cAMP attenuates the lung injury by cold preservation and ischemia-reperfusion, at least partly by protection of the vascular endothelium.

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